Claus-Dieter Gerharz

Heinrich-Heine-Universität Düsseldorf, Düsseldorf, North Rhine-Westphalia, Germany

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Publications (8)50.19 Total impact

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    ABSTRACT: Gorham-Stout disease is an unusual, progressive syndrome of unknown etiology characterized by mono- or polyostotic osteolysis most often affecting children and young adults. The onset is insidious and the disease progresses to extensive and potentially disabling osteolysis often unresponsive to therapeutic intervention. Although bone and soft tissue lesions are the most frequent manifestations of Gorham-Stout disease, skin lesions can occur and may provide a clue to the pathogenesis of this rare syndrome. Our aim was to describe characteristics of vascular skin lesions of this rare condition using magnetic resonance imaging and histomorphological analysis. The case of a 36-year-old man with Gorham-Stout disease of the left leg and foot is reported. This case was remarkable for its prominent lymphatic vascular malformations involving the skin and soft tissues adjacent to the diseased bone-a previously undescribed abnormality, which preceded osteolysis for several years. Magnetic resonance imaging played a key role in defining the extent of disease in skin and soft tissues. It is difficult to assess the true incidence of hemangiomatosis in the earlier reports on Gorham-Stout disease in which hemangiomatous cutaneous lesions were mentioned but not described or illustrated. A vascular process with angiomatous histological features is considered to be the pathological hallmark of Gorham-Stout disease, but the specific type of this vascular process is still under debate. Our report highlights a lymphatic malformative nature of Gorham-Stout disease, thereby contributing to a better understanding and characterization of this rare disease entity.
    Journal of the American Academy of Dermatology 03/2007; 56(2 Suppl):S21-5. · 4.91 Impact Factor
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    ABSTRACT: Penile metastases are rare and are considered to reflect end-stage malignant disease. The first case of a follicular thyroid carcinoma metastasizing to the penis is described. Local tumor control and probably enhanced survival was achieved by extended surgery of a previous pelvic recurrence and the penile metastasis and this procedure may be justified in selected cases.
    Scandinavian Journal of Urology and Nephrology 02/2004; 38(3):253-5. · 1.01 Impact Factor
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    ABSTRACT: In many common cancers such as transitional cell carcinoma (TCC), specific genes are hypermethylated, whereas overall DNA methylation is diminished. Genome-wide DNA hypomethylation mostly affects repetitive sequences such as LINE-1 retrotransposons. Methylation of these sequences depends on adequate expression of DNA methyltransferase I (DNMT1) during DNA replication. Therefore, DNMT1 expression relative to proliferation was investigated in TCC cell lines and tissue as well as in renal carcinoma (RCC) cell lines, which also display hypomethylation, as indicated by decreased LINE-1 methylation. Cultured normal uroepithelial cells or normal bladder tissue served as controls. In all tumor cell lines, DNMT1 mRNA as well as protein was decreased relative to the DNA replication factor PCNA, and DNA hypomethylation was present. However, the extents of hypomethylation and DNMT1 downregulation did not correlate. Reporter gene assays showed that the differences in DNMT1 expression between normal and tumor cells were not established at the level of DNMT1 promoter regulation. Diminished DNMT1:PCNA mRNA ratios were also found in 28/45 TCC tissues but did not correlate with the extent of DNA hypomethylation. In addition, expression of the presumed de novo methyltransferases DNMT3A and DNMT3B mRNAs was investigated. DNMT3B overexpression was observed in about half of all high-stage TCC (DNMT3B vs. tumor stage, chi(2): p = 0.03), whereas overexpression of DNMT3A was rarer and less pronounced. Expression of DNMT3A and DNMT3B in most RCC lines was higher than in TCC lines. Our data indicate that DNMT1 expression does not increase adequately with cell proliferation in bladder cancer. This relative downregulation probably contributes to hypomethylation of repetitive DNA but does not determine its extent alone.
    International Journal of Cancer 06/2003; 104(5):568-78. · 6.20 Impact Factor
  • JAMA The Journal of the American Medical Association 04/2003; 289(12):1479-80. · 29.98 Impact Factor
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    ABSTRACT: p27Kip1 (p27) protein is an inhibitor of cyclin-dependent kinase complexes and prevents progression of cells from the G1- to the S-phase of the cell cycle. Decreased p27 expression has been shown to be associated with aggressive tumor behavior and decreased patient survival in numerous human malignancies. The aim of this study was to evaluate p27 expression in renal cell cancer and to assess its association with stage and grade as well as its relationship to patient outcome. One hundred and fifty-four renal cell carcinoma specimens were evaluated for p27 expression by immunohistochemical staining. Immunohistochemical findings were correlated with tumor grade, tumor stage and patient outcome. A progressive loss of nuclear p27 expression was observed with increasing tumor grade. In poorly-differentiated tumors, p27 expression was significantly lower compared to well- and moderately-differentiated tumors (p = 0.025). p27 expression tended to decrease with increasing tumor stage, but the correlation was not statistically significant (p = 0.068). The present study suggests that renal cell carcinomas showed increased aggressiveness with loss of p27 expression. A longer follow-up period will demonstrate whether this cell cycle regulator will provide additional prognostic information in patients with renal cell carcinoma.
    Anticancer research 01/2003; 23(1A):217-21. · 1.71 Impact Factor
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    ABSTRACT: To evaluate the expression of p27(KIP1) and p21(CIP1) and the prognostic values of both markers in urothelial carcinoma. The expression of the cyclin-dependent kinase inhibitor p27(KIP1) characterizes early-stage and well-differentiated carcinomas of the colon, breast, and prostate and is associated with an improved prognosis. In urothelial carcinoma, its expression has not been as well investigated. Another cyclin-dependent kinase inhibitor, p21(CIP1), is expressed in early-stage bladder tumors, but published data on its prognostic value are contradictory. Expression of p27(KIP1) and p21(CIP1) was analyzed by immunohistochemistry in 114 urothelial carcinoma specimens from 77 patients. The Ki67 index was determined as an indicator of cell proliferation. The expression of the markers was correlated with tumor recurrence and progression during an average follow-up period of 3.9 years. Expression of p27(KIP1) was significantly more frequent in superficial than in muscle-invasive tumors (chi-square test, P = 0.012; Fisher's exact test, P = 0.014). Although similar overall, the expression pattern of p21(CIP1) did not match on a tumor-by-tumor basis. No correlation was seen with the Ki67 index. Patients with tumors displaying strong positive staining for p27(KIP1) or p21(CIP1) had fewer recurrences and progression events, but the difference was not statistically significant. Instead, a Ki67 index of less than 10% was significantly (P = 0.0335) related to a lack of recurrence. Neither p27(KIP1) nor p21(CIP1) appear to be good predictors of tumor progression in urothelial carcinoma, even though their expression is strongly decreased in muscle-invasive tumors.
    Urology 11/2000; 56(4):689-95. · 2.42 Impact Factor
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    ABSTRACT: Alterations of the CDKN2A locus on chromosome 9p21 encoding the p16INK4A cell cycle regulator and the p14ARF1 p53 activator proteins are frequently found in bladder cancer. Here, we present an analysis of 86 transitional cell carcinomas (TCC) to elucidate the mechanisms responsible for inactivation of this locus. Multiplex quantitative PCR analysis for five microsatellites around the locus showed that 34 tumors (39%) had loss of heterozygosity (LOH) generally encompassing the entire region. Of these, 17 tumors (20%) carried homozygous deletions of at least one CDKN2A exon and of flanking microsatellites, as detected by quantitative PCR. Analysis by restriction enzyme PCR and methylation-specific PCR showed that only three specimens, each with LOH across 9p21, had bona fide hypermethylation of the CDKN2A exon 1 CpG-island in the remaining allele. Like most other specimens, these three specimens displayed substantial genome-wide hypomethylation of DNA as reflected in the methylation status of LINE L1 sequences. The extent of DNA hypomethylation was significantly more pronounced in TCC with LOH and/or homozygous deletions at 9p21 than in those without (26% and 28%, respectively, on average, versus 11%, p < 0.0015). No association of LOH or homozygous deletions at 9p21 with tumor stage or grade was found. The data indicate that DNA hypermethylation may be rare in TCC and that deletions are the most important mechanism for inactivation of the CDKN2A locus. The predominance of allelic loss may be explained by its correlation with genome-wide DNA hypomethylation, which is thought to favor chromosomal instability and illegitimate recombination.
    Laboratory Investigation 09/2000; 80(10):1513-1522. · 3.96 Impact Factor
  • Journal of Urology - J UROL. 01/1999; 162(5).